The purpose of the proposed project is to investigate changes in renal function and fluid balance during acute and chronic neurogenic hypertension in the rat. In one series of experiments, neurogenic hypertension will be produced by selective aortic baroreceptor deafferentation (ABD) in rats. Subsequently, steady-state renal functions, and renal and hemodynamic responses to acute and chronic volume loading, will be compared in conscious ABD and normotensive control rats. Additional studies will seek to ascertain the mechanism ofABD-induced alterations in body fluid balance, and test the theory that the degree of hypertension produced by ABE is determined by intrinsic differences in the fluid handling capacity of individual animals. The role of body fluid regulatory mechanisms in two other putative forms of "neurogenic hypertension" will also be similarly investigated: 1) chronic electrical stimulation of the hypothalamus in conscious rats, and 2) chronic intravenous infusion into conscious rats of the sympathetic neurotransmitter, norepinephrine. In most of these experiments, simultaneous measurement of fluid balance and hemodynamic variables will help clarify the degree to which alterations in body salt and water content influence arterial pressure via changes in cardiac output, as opposed to doing so via changes in peripheral vascular resistance. The ultimate goal of this work is to understand why the increased neurogenic cardiovascular activity observed in a large number of mainly young "borderline" hypertensive humans appears to lead later to stable "essential" hypertension in some of these individuals but not in others. Since our preliminary work, and published studies of many other investigators, indicate that the final steady-state blood pressure in experimental neurogenic hypertension is also quite variable from individual-to-individual, this experimental paradigm will be used as a model for the human situation. The hypothesis to be tested is that the chronic blood pressure level achieved in response to neurogenic cardiovascular stimulation is determined at least in part by the reactin of bodyfluid regulatory systems to such stimulation.